Relevant bibliographies by topics / T cells responses

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'T cells responses'

Author: Grafiati
Published: 14 March 2023

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Journal articles on the topic "T cells responses"

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Tadokoro, Carlos E., Guy Shakhar, Shiqian Shen, et al. "Regulatory T cells inhibit stable contacts between CD4+ T cells and dendritic cells in vivo." Journal of Experimental Medicine 203, no. 3 (2006): 505–11. http://dx.doi.org/10.1084/jem.20050783.

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Regulatory T (T reg) cells exert powerful down-modulatory effects on immune responses, but it is not known how they act in vivo. Using intravital two-photon laser scanning microscopy we determined that, in the absence of T reg cells, the locomotion of autoantigen-specific T cells inside lymph nodes is decreased, and the contacts between T cells and antigen-loaded dendritic cells (DCs) are of longer duration. Thus, T reg cells can exert an early effect on immune responses by attenuating the establishment of stable contacts during priming of naive T cells by DCs.
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Krawczyk, Connie M., Hao Shen, and Edward J. Pearce. "Memory CD4 T Cells Enhance Primary CD8 T-Cell Responses." Infection and Immunity 75, no. 7 (2007): 3556–60. http://dx.doi.org/10.1128/iai.00086-07.

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ABSTRACT CD4 T-cell help is required for optimal memory CD8 T-cell responses. We have found that engaging preexisiting CD4 Th1, but not Th2, memory cells at the time of CD8 T-cell priming results in increased CD8 effector responses to both bacterial and viral pathogens. The enhanced responses are characterized by increased numbers of cytokine-producing, antigen-specific cells. These findings suggest that engaging endogenous memory Th1 cells may increase cellular responses in an immunotherapy or vaccination setting.
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Jiang, Xiaodong, Rachael Clark, Luzheng Liu, et al. "CD4+ T cells regulate skin resident memory CD8+ T cells (TRM) (49.8)." Journal of Immunology 188, no. 1_Supplement (2012): 49.8. http://dx.doi.org/10.4049/jimmunol.188.supp.49.8.

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Abstract The requirement of CD4+ T cell help for CD8+ T cell responses has been extensively explored in secondary lymphoid organs using systemic infection models. Whether such help also exists in peripheral tissues like the skin is unknown. We recently reported that skin resident memory CD8+ T cells (TRM) are non-recirculating and are superior to central memory CD8+ T cells (TCM) in protecting against re-infection. Interestingly, we also found that the acute CD8+ T cell migration into infected skin does not require CD4+ T cell help. Further study showed that the acute protection response of CD8+ T cells in the skin was equivalent in wild type and CD4-deficient mice. We next asked the role of CD4+ T cells in CD8+ TRM protective responses in the skin. To our surprise, the absence of CD4+ T cells did not impair the survival of CD8+ TRM in the skin. However, the recall response of CD8+ TRM in previously infected skin was significantly compromised in CD4-/- mice. The viral load assay further showed that the recall response of CD8+ TRM was significantly compromised when memory CD4+ T cells in the skin were depleted, suggesting that signals from memory CD4+ T cells in the skin are delivered to CD8+ TRM locally. Taken together, these data imply that while CD4+ T cells are not required both for acute CD8+ T cell response and maintenance CD8+ TRM in the skin, they do play an important role in regulating recall responses of CD8+ TRM.
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Chauhan, Priyanka, Shuxian Hu, Wen S. Sheng, and James R. Lokensgard. "Regulatory T-Cells Suppress Cytotoxic T Lymphocyte Responses against Microglia." Cells 11, no. 18 (2022): 2826. http://dx.doi.org/10.3390/cells11182826.

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Regulatory T-cells (Tregs) play pivotal roles during infection, cancer, and autoimmunity. In our previous study, we demonstrated a role for the PD-1:PD-L1 pathway in controlling cytolytic responses of CD8+ T lymphocytes against microglial cells presenting viral peptides. In this study, we investigated the role of Tregs in suppressing CD8+ T-cell-mediated cytotoxicity against primary microglial cells. Using in vitro cytotoxicity assays and flow cytometry, we demonstrated a role for Tregs in suppressing antigen-specific cytotoxic T-lymphocyte (CTL) responses against microglia loaded with a model peptide (SIINFEKL). We went on to show a significant decrease in the frequency of IFN-γ- and TNF-producing CD8+ T-cells when cultured with Tregs. Interestingly, a significant increase in the frequency of granzyme B- and Ki67-producing CTLs was observed. We also observed a significant decrease in the production of interleukin (IL)-6 by microglia. On further investigation, we found that Tregs significantly reduced MHC class 1 (MHC-1) expression on IFN-γ-treated microglial cells. Taken together, these studies demonstrate an immunosuppressive role for Tregs on CTL responses generated against primary microglia. Hence, modulation of Treg cell activity in combination with negative immune checkpoint blockade may stimulate anti-viral T-cell responses to more efficiently clear viral infection from microglial cell reservoirs.
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Weis-Banke, Stine Emilie, Thomas Landkildehus Lisle, Maria Perez-Penco, et al. "Arginase-2-specific cytotoxic T cells specifically recognize functional regulatory T cells." Journal for ImmunoTherapy of Cancer 10, no. 10 (2022): e005326. http://dx.doi.org/10.1136/jitc-2022-005326.

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BackgroundHigh expression of the metabolic enzyme arginase-2 (ARG2) by cancer cells, regulatory immune cells, or cells of the tumor stroma can reduce the availability of arginine (L-Arg) in the tumor microenvironment (TME). Depletion of L-Arg has detrimental consequences for T cells and leads to T-cell dysfunction and suppression of anticancer immune responses. Previous work from our group has demonstrated the presence of proinflammatory ARG2-specific CD4 T cells that inhibited tumor growth in murine models on activation with ARG2-derived peptides. In this study, we investigated the natural occurrence of ARG2-specific CD8 T cells in both healthy donors (HDs) and patients with cancer, along with their immunomodulatory capabilities in the context of the TME.Materials and methodsA library of 15 major histocompatibility complex (MHC) class I-restricted ARG2-derived peptides were screened in HD peripheral blood mononuclear cells using interferon gamma (IFN-γ) ELISPOT. ARG2-specific CD8 T-cell responses were identified using intracellular cytokine staining and ARG2-specific CD8 T-cell cultures were established by enrichment and rapid expansion following in vitro peptide stimulation. The reactivity of the cultures toward ARG2-expressing cells, including cancer cell lines and activated regulatory T cells (Tregs), was assessed using IFN-γ ELISPOT and a chromium release assay. The Treg signature was validated based on proliferation suppression assays, flow cytometry and quantitative reverse transcription PCR (RT-qPCR). In addition, vaccinations with ARG2-derived epitopes were performed in the murine Pan02 tumor model, and induction of ARG2-specific T-cell responses was evaluated with IFN-γ ELISPOT. RNAseq and subsequent GO-term and ImmuCC analysis was performed on the tumor tissue.ResultsWe describe the existence of ARG2-specific CD8+T cells and demonstrate these CD8+T-cell responses in both HDs and patients with cancer. ARG2-specific T cells recognize and react to an ARG2-derived peptide presented in the context of HLA-B8 and exert their cytotoxic function against cancer cells with endogenous ARG2 expression. We demonstrate that ARG2-specific T cells can specifically recognize and react to activated Tregs with high ARG2 expression. Finally, we observe tumor growth suppression and antitumorigenic immunomodulation following ARG2 vaccination in an in vivo setting.ConclusionThese findings highlight the ability of ARG2-specific T cells to modulate the immunosuppressive TME and suggest that ARG2-based immunomodulatory vaccines may be an interesting option for cancer immunotherapy.
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Wong, Wei. "Activating T cells with asparagine." Science Signaling 14, no. 668 (2021): eabg8244. http://dx.doi.org/10.1126/scisignal.abg8244.

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Olson, Matthew, and Stephen Turner. "CD4 T cells license dendritic cells to enhance polyfunctional anti-viral T helper cell responses (P6094)." Journal of Immunology 190, no. 1_Supplement (2013): 173.3. http://dx.doi.org/10.4049/jimmunol.190.supp.173.3.

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Abstract CD4 T cell help is critical for the generation of optimal B cell and CD8 T cell responses after immunization or infection. Robust and polyfunctional CD4 T cells are also generated after exposure to antigen, however, the factors that govern the development of potent CD4 T cell immunity are less clear. We demonstrate here that augmenting CD4 T cell help by adoptive transfer of increasing numbers of influenza A virus (IAV)-specific T cell receptor transgenic T cells resulted in enhanced polyclonal IAV-specific CD4 T cell responses after infection. Virus-specific CD4 T cells in mice that received augmented help also exhibited a greater capacity to produce multiple cytokines as compared to controls, indicating that CD4 T cell help is a major factor that dictates CD4 T cell polyfunctionality. Mechanistically, CD154 expression on CD4 T cells and CD40 on dendritic cells (DCs) were both necessary and sufficient to induce optimal CD4 T cell responses after infection, suggesting that helper T cells “license” DCs to enhance CD4 T cell responses. Interestingly, augmenting CD4 T cell help also resulted in enhanced IAV-specific CD4 and CD8 T cell memory responses after secondary infection. Taken together, these data define a CD4 T cell-DC circuit that promotes the priming of robust and polyfunctional CD4 T cell responses. These data also suggest that enhancing CD4 T cell help during vaccination could be used as a therapeutic approach to promote overall T cell immunity.
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Schilbach, Karin, Hendrik Ziegler, Jan Haarer, Marco Sterk, Hans-Georg Rammensee та Rupert Handgretinger. "Human peripheral Vδ1+ γδ T cells can develop into αβ T cells (P4460)". Journal of Immunology 190, № 1_Supplement (2013): 52.47. http://dx.doi.org/10.4049/jimmunol.190.supp.52.47.

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Abstract The T cell compartment can be divided in two large classes: αβ and γδ T cells. It is believed that they develop in the thymus from a common progenitor and that the choice between αβ and γδ T cell fate is the first lineage decision made by progenitors after they commit to the T-cell lineage. However, here we show that peripheral Vδ1+ γδ T cells in an inflammatory environment can transdifferentiate into αβ T cells. Upon their extrathymic route of differentiation, that resembles well-characterized molecular program of thymic αβ lineage development, Vδ1+ T cells upregulate CD4+ coreceptor, develop Vδ1+ CD4+CD8+ double positive cells, show heterodimeric CD8αβ, transcribe RAG, preTα and express a particular Vβchain on their surface. Simultaneously inflammation confers controlled initiation of rearrangement in the TCRα locus. Transdifferentiation of Vδ1+ T cells at the clonal and bulk-culture level into functional CD4+ or CD8+ αβ T cells via a Vδ1+TCR/αβ+TCR double positive stage suggests that, upon inflammatory stimuli, Vδ1+ T-cell conversion participates in the induction of adaptive immune responses. Identifying an innate T cell as an αβ T-cell progenitor and showing the developmental steps linking the progenitor to adaptive, thymus-independant αβ T-cell responses as inflammatory conditions is of utmost relevance and will deeply impact evaluation of immune responses in infection, malignancy and autoimmune processes.
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Plitas, George, and Alexander Y. Rudensky. "Regulatory T Cells in Cancer." Annual Review of Cancer Biology 4, no. 1 (2020): 459–77. http://dx.doi.org/10.1146/annurev-cancerbio-030419-033428.

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The immune system has evolved complex effector mechanisms to protect the host against a diversity of pathogenic organisms and regulatory adaptations that can curtail pathological sequelae of inflammatory events, prevent autoimmunity, and assist in tissue repair. Cancers, by virtue of their local manifestations of tissue dysfunction and destruction, inflammation, and genomic instability, can evoke these protective mechanisms, which support the progression of tumors and prevent their immune eradication. Central to these processes is a subset of CD4+ T cells, known as regulatory T (Treg) cells, that express the X chromosome–linked transcription factor FOXP3. In addition to their critical role in controlling autoimmunity and suppressing inflammatory responses in diverse biological settings, Treg cells are ubiquitously present in the tumor microenvironment where they promote tumor development and progression by dampening antitumor immune responses. Furthermore, Treg cells can directly support the survival of transformed cells through the elaboration of growth factors and interacting with accessory cells in tumors such as fibroblasts and endothelial cells. Current insights into the biology of tumor-associated Treg cells have opened up opportunities for their selective targeting in cancer, with the goal of alleviating their suppression of antitumor immune responses while maintaining overall immune homeostasis.
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Kursar, Mischo, Kerstin Bonhagen, Joachim Fensterle, et al. "Regulatory CD4+CD25+ T Cells Restrict Memory CD8+ T Cell Responses." Journal of Experimental Medicine 196, no. 12 (2002): 1585–92. http://dx.doi.org/10.1084/jem.20011347.

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CD4+ T cell help is important for the generation of CD8+ T cell responses. We used depleting anti-CD4 mAb to analyze the role of CD4+ T cells for memory CD8+ T cell responses after secondary infection of mice with the intracellular bacterium Listeria monocytogenes, or after boost immunization by specific peptide or DNA vaccination. Surprisingly, anti-CD4 mAb treatment during secondary CD8+ T cell responses markedly enlarged the population size of antigen-specific CD8+ T cells. After boost immunization with peptide or DNA, this effect was particularly profound, and antigen-specific CD8+ T cell populations were enlarged at least 10-fold. In terms of cytokine production and cytotoxicity, the enlarged CD8+ T cell population consisted of functional effector T cells. In depletion and transfer experiments, the suppressive function could be ascribed to CD4+CD25+ T cells. Our results demonstrate that CD4+ T cells control the CD8+ T cell response in two directions. Initially, they promote the generation of a CD8+ T cell responses and later they restrain the strength of the CD8+ T cell memory response. Down-modulation of CD8+ T cell responses during infection could prevent harmful consequences after eradication of the pathogen.
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Dissertations / Theses on the topic "T cells responses"

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Crawford, A. "How B cells influence T cell responses." Thesis, University of Edinburgh, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.645118.

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Although studies using B cell deficient mice have been useful in understanding the importance of B cells under different conditions, it is difficult to then dissect exactly how B cells could be regulating T cell responses. By transferring OT-II transgenic T cells into either B cell deficient (μMT) or C57BL/6 mice, expansion and contraction of T cells can be tracked <i>ex vivo. </i>Expansion of OT-II cells is reduced in μMT mice compared to C57BL/6 mice. Thus, B cells can provide costimulatory signals, secrete cytokines and influence the lymphoid microarchitecture. To dissect which B cell factor(s) are involved in enhancing OT-II T cell expansion, a model system was used where one molecule on the B cells is depleted at one time. This was achieved by creating bone-marrow chimeras using a combination of μMT bone-marrow and wildtype or deficient bone-marrow. Thus, all the B cells are either wildtype or deficient for a particular molecule. The molecules examined were MHC-II, which is required for antigen presentation, CD40, due to its costimulatory role, and lymphotoxin-alpha, for its role in maintenance of splenic architecture. Using the OT-II adoptive transfer system, we have shown a requirement for MHC-II but not CD40 on B cells for efficient T cell expansion. In light of these observations, the role of B cell-derived MHC-II for T cell memory generation was examined. To do this, I used MHC-II tetramers to track a polyclonal population of T cells in the host.  Using this technique, I have shown that T cell memory is also diminished when the B cells do not express MHC-II. Thus, a cognate interaction with B cells is required for both efficient expansion and memory generation of CD4<sup>+</sup> T cells.
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Crawford, Alison. "Role of B cells in influencing T cell responses." Thesis, University of Edinburgh, 2004. http://hdl.handle.net/1842/13483.

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Smith, Trevor Robert Frank. "Modulation of CD4+ T cell responses by CD4+CD25+ regulatory T cells and modified T cell epitopes." Thesis, Imperial College London, 2004. http://hdl.handle.net/10044/1/11317.

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Preciado-Llanes, Lorena. "Inhibition of T-cell responses by microbes and immune cells." Thesis, University of Sheffield, 2013. http://etheses.whiterose.ac.uk/4717/.

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Some antigens can induce B-cell activation and antibody production without 'T cell help' and hence are called T-independent (TI) antigens. Similarly to bacterial capsular polysaccharides, anti- IgDconjugated dextran (α-δ-DEX) is a TI type 2 mimic which stimulates B lymphocytes by crosslinking of numerous B-cell receptor molecules. This thesis demonstrates that α-δ-DEX-activated B-cells directly inhibit TCR-induced CD4+ T-cell proliferation and activation in vitro. Experiments performed with purified cell populations excluded the possibility of α-δ-DEX acting directly on CD4+ T lymphocytes and confirmed that B lymphocytes exposed to α-δ-DEX for a period of 24 hours become activated and acquire a suppressive phenotype. Interestingly, these suppressor Bcells appear to be effective even when they are present at numbers below the physiological T:B ratio. Although the exact mechanism of action remains obscure, this is the first evidence of TI type 2 antigen activated B-cells mediating inhibition of activation and proliferation of helper T lymphocytes. Neisseria meningitidis is a bacterium which rarely causes invasive disease and sepsis, but perpetuates colonisation in the nasopharynx by avoiding immune recognition and killing. Because several N. meningitidis constituents are TI type 2 antigens and/or provide second signals to B-cells via TLRs, it was hypothesized that paraformaldehyde fixed meningococcus could exert immunomodulatory properties. A deep suppression of CD4+ T-cell responses occurred when aCD3-stimulated PBMCs where incubated with small meningococci counts (ratios between 0.1 to 10:1 bacteria per cell). A clear TH1 cytokine profile and IL-10 secretion was observed in supernatants from these cultures. Interestingly, outer membrane vesicles (OMVs) from N. meningitidis and N. lactamica replicated the suppression phenomenon induced by the whole organism. Bacterial capsule, lipooligosaccharides and Opa are not responsible for the suppressive effect. Depletion of B-cells, monocytes or NK cells does not reverse the meningococcus-mediated inhibition in PBMC cultures. Several bacterial components stimulate nitric oxide (NO) production, however N. meningitidis can counteract the bactericidal effect of reactive nitrogen intermediates by a partial denitrification pathway. Since NO is also produced as a result of TCR engagement, it was investigated whether NO donation or inhibition could influence CD4+ T-cell responses. A novel specific eNOS inhibitor (Cavtratin) derived from the caveolin-1 structure was tested for the first time in PBMC cultures. Cavtratin concentrations of 10 and 15 μM increases proliferation of CD4+ T lymphocytes and reduce the percentage of cell death in the PBMC culture after anti-CD3 stimulation.
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Barroso, Herrera Osquel Miguel. "Manipulation of antigen-specific T cell responses by modified dendritic cells." Thesis, Imperial College London, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.405941.

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Li, Xiaoying. "T cell receptor repertoires of immunodominant CD8 T cell responses to Theileria parva." Thesis, University of Edinburgh, 2015. http://hdl.handle.net/1842/19552.

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Previous research has provided evidence that CD8 T cells mediate immunity against infection with Theileria parva. However, the immunity induced by one parasite strain doesn‟t give complete protection against other strains and this is associated with parasite strain specificity of the CD8 T cell responses. There is evidence that such strain specificity is a consequence of the CD8 T cell responses of individual animals being focused on a limited number of immunodominant polymorphic peptide-MHC determinants. Dominant responses to the Tp2 antigen have been demonstrated in animals homozygous for the A10 MHC haplotype. Three Tp2 epitopes recognised by A10+ animals (Tp249-59, Tp250-59 and Tp298-106) have been defined. This project set out to investigate the dominance of these epitopes and to examine the T cell receptor (TCR) repertoires of the responding T cells. The specific objectives were to: (i) Determine the dominance hierarchies of the three defined Tp2 epitopes in both A10-homozygous and -heterozygous cattle. (ii) Examine the clonal repertoires of epitope-specific responses by analysis of TCR gene expression. (iii) Isolate full-length cDNAs encoding TCR α and β chain pairs from T cell clones of defined epitope specificity and use them to generate cells expressing the functional TCRs. Using MHC class I tetramers the relative dominance of CD8 T cell responses were found to differ between A10-homozygous and heterozygous cattle. All A10-homozygous cattle examined had detectable responses to all 3 Tp2 epitopes, the Tp249-59 epitope consistently being the most dominant. By contrast, only some A10-heterozygous cattle had detectable responses to Tp2 and when present the response was specific only for the Tp298-106 epitope. Analyses of the sequences of expressed TCR β chains showed that the responses in individual animals were clonotypically diverse, but often contained a few large expanded clonotypes. The TCRs of Tp298-106–specific T cells showed preferential usage of the Vβ13.5 gene and the frequent presence of a “LGG” motif within the CDR3 of the B chain. A conserved (public) TCRβ clonotype shared by the Tp250-59-specific CD8 T cells from all A10-homozygous cattle was identified. The TCRα chains co-expressed with this public TCRβ clonotype were identified for a number of T cell clones. Lentivirus transduction of Jurkat cells with three full-length TCR α and β chain pairs resulted in successful expression of one of the α/β chain pairs as a functional TCR, thus providing the basis for future work to generate bovine T cells expressing defined TCRs in vitro.
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Wangteeraprasert, Apirath. "CD8+ T-cells responses in Dengue virus infection." Thesis, Imperial College London, 2012. http://hdl.handle.net/10044/1/39398.

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Dengue virus, which has four serotypes, has several clinical manifestations including asymptomatic infection, a self-limiting febrile illness termed dengue fever (DF) and a severe form characterized by plasma leakage termed dengue hemorrhagic fever (DHF). The pathogenesis of DHF is not fully understood and many studies have shown that it is more prevalent during secondary infection. In addition to a mechanism termed antibody dependent enhancement (ADE), the role of T-cells in the pathogenesis of dengue also has been investigated. It has been hypothesized that upon secondary infection dengue-specific memory T-cells generated during a previous infection, which are cross-reactive and have low avidity for the current serotype dominate the T-cell response. This phenomenon is called 'Original antigenic sin' and the consequence of this low avidity T-cell response may be ineffective viral elimination leading to increased production of inflammatory cytokines which could cause plasma leakage. To study CD8+ T-cell responses to dengue-peptide variants, HLA-A11-restricted NS3 133-142-specific T-cell clones were generated and their cytotoxicity, proliferation and cytokine production in response to variant epitopes was tested. The results support that the magnitude of T-cell responses is related to the strength of the TCR-peptide-MHC interaction. AG129 mice, which lack both IFN (symbol missing) and IFN (symbol missing) receptors, show susceptibility to dengue virus infection and develop symptoms seen during human infection such as vascular leakage. This allows for investigation of the role of T-cell responses generated towards sequential infections with well defined serotypes. Experiments that would be very difficult to carry out in human dengue patients. Splenocytes from sequentially infected AG129 mice were assayed for their response to whole dengue proteins from serotype 1 and 2 virus. New epitopes were identified and CD8+ T-cell lines and clones were generated and their functions studied using peptide variants. The results showed that dengue-specific cross-reactive memory CTLs displayed better recognition of epitopes encountered during primary immunisa tion as compare to those recognised during secondary immunisation, which supports the idea of original antigenic sin in dengue-specific CD8+ T -cells. In conclusion, this study focuses on cross-reactive dengue-specific CD8+ T-cells and their functions when recognizing heterologous dengue peptides to clarify their role in pathogenesis.
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Deng, Jun, and 鄧軍. "Leptin modulates T cells responses in autoimmune arthritis." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2014. http://hdl.handle.net/10722/208601.

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Leptin, a protein hormone encoded by obese (ob) gene, is mainly produced by adipocytes. Leptin plays an important role in regulating neuroendocrine function and energy metabolism. As a cytokine, leptin is involved in modulating the hematopoiesis and lymphopoiesis. Although leptin has been found to promote T cells activation, it is largely unclear whether and how leptin regulates T cell differentiation and function. Leptin has been associated with disease severity in rheumatoid arthritis (RA). Elevated leptin levels have been detected in the sera and synovial fluid of active RA patients. Th17 cells play key roles in synovitis and joint damage during arthritis development. However, the role of leptin on Th17 cells has not been investigated so far. In culture, leptin promoted Th17 cells differentiationfrom naïve 〖CD4〗^+ T cells via upregulating ROR-γt expression. Moreover, Th17 cells and IL-17 levels were significantly increased in leptin-treated naïve CD4+ T cells. Moreover, this study found that synoviocytes and chondrocytes produced large amounts of leptin especially during acute and chronic stages of mice with collagen-induced arthritis (CIA). Furthermore, leptin levels, Th17 cells in the joint and IL-17 levels in the synovial fluid were closely related to disease activity. Leptin intraarticular injection led to earlier onset of disease, higher clinical score, and more severe joint destruction compared with PBS-treated control mice. Importantly, leptin-injected mice had higher percentages of Th17 cells and cell numbers, elevated IL-17 levels in the synovial fluid, and increased infiltration of Th17 cells in the inflamed joint tissues compared with PBS-treated mice. T follicular helper (Tfh) cells are indispensible for pathogenic autoantibodies production. However, whether leptin receptor (ObR) signaling has a role on Tfh cells and its implication in CIA remain elusive. Upon a T cell-dependent antigen TNP-KLH immunization, germinal center (GC) response, plasma cells (PCs) and memory B cells formation were impaired in db/db mice compared with wild-type (WT) controls. In coculture of Tfh cells from db/db and WT mice with WT GC B cells, anti-TNP IgGs titers in supernatants of db/db Tfh cells were significantly reduced. Intravenously transfer of naïve CD4+ T cells from db/db and WT mice to BoyJ recipient mice, donor CD4+ T cells from db/db mice showed impaired Tfh cells generation in spleens of BoyJ recipient mice compared with mice received with WT CD4+ T cells. These data indicated that ObR-mediated signaling intrinsically modulate Tfh cells generation. In culture, leptin promoted Tfh cells differentiation via inducing Bcl6 expression, and increased IL-21 production in Tfh cells in a dose-dependent manner. Leptin significantly enhanced the phosphorylation of STAT3, upregulated Bcl6 expression, and increased p-STAT3 binding to the Il21 promoter in CD4+ T cells with leptin receptor b (Ob-Rb) overexpression. Upon CIA induction, db/db mice exhibited ameliorated disease severity with impaired Tfh cells response. However, WT Tfh cells transfer to db/db mice restored GC responses, PCs formation, antibody production, and exacerbated synovium inflammation and joint damage in db/db recipient mice. Together, these findings demonstrate that leptin modulates arthritis development via enhancement of Th17 and Tfh cells responses.<br>published_or_final_version<br>Pathology<br>Doctoral<br>Doctor of Philosophy
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Sutherland, Andrew Peter Robert St Vincents Clinical School UNSW. "BAFF regulation of peripheral T cell responses." Awarded by:University of New South Wales. St Vincents Clinical School, 2005. http://handle.unsw.edu.au/1959.4/22788.

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The activation and effector function of CD4+ T cells are critical points of regulation during an antigen specific T cell response. Dysregulation of these processes can lead to the development of human diseases, encompassing both immunodeficiency and autoimmunity. Members of the TNF superfamily have recently emerged as important regulators of T cell responses, with their overexpression causing autoimmune inflammation in animal models. As overproduction of the novel TNF superfamily ligand BAFF is associated with several autoimmune conditions, we sought to examine the potential role of BAFF as a regulator of T cell activation and effector function. We initially demonstrated BAFF costimulation of T cell activation in vitro. Generation of specific monoclonal antibodies identified BAFF-R as the only BAFF receptor present on T cells, and showed that it was expressed in an activation-dependent and subset-specific manner. Impaired BAFF costimulation in BAFF-R deficient mice indicated that BAFF-R was crucial for mediating BAFF effects in T cells. Analysis of T cell responses in vivo revealed that BAFF transgenic mice have increased T cell priming and recall responses to protein antigens, and showed a corresponding increase in the DTH model of Th1 cell-dependent inflammation. In addition, Th2-dependent allergic airway responses are suppressed in BAFF transgenic mice. Crossing to a B cell deficient background revealed that the proinflammatory effects of BAFF on T cell priming and DTH rely on the presence of B cells, while the suppressive effects during allergic airway inflammation are B cell independent. These data demonstrated that BAFF regulated the outcome of T cell responses in vivo and identified BAFF dependent crosstalk between T and B cells. Stimulation of B cells with BAFF induced the upregulation of MHC class II and ICOS-L both in vitro and in vivo. Induction of these cell surface molecules was associated with an increased capacity to induce T cell proliferation, however this effect was independent of ICOS-L expression. Thus it was demonstrated that BAFF regulated T cell activation and effector function both directly, via stimulation of BAFF-R, and indirectly, by altering the function of B cells. These data suggest that BAFF dependent alterations in T cell function may be an additional causative factor in the association between elevated BAFF levels and the generation of autoimmunity.
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Easterfield, Alistair John. "Foetal modulation of maternal T lymphocyte responses." Thesis, St George's, University of London, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.325057.

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Books on the topic "T cells responses"

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Tomkins, Paul Thomas. Interferon modulation of T-cell responses to Semliki Forest virus infected murine brain cells. typescript, 1989.

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Dockery, Dee. T cell responses to OspA, a candidate Lyme Disease vaccine. s.n.], 1993.

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Nagorsen, Dirk, and F. M. Marincola, eds. Analyzing T Cell Responses. Springer Netherlands, 2005. http://dx.doi.org/10.1007/1-4020-3623-x.

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Brouwenstijn, Nathalie. Characterization of the T-cell mediated immune response to renal cell carcinoma. University of Leiden], 1998.

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Regulatory T cells: Methods and protocols. Humana Press, 2011.

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Liu, Yang. The costimulatory pathway for T cell response. R.G. Landes, 1994.

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L, Edelson Richard, ed. Antigen and clone-specific immunoregulation. New York Academy of Sciences, 1991.

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Na, Songqing, and Chandrasekar Venkataraman Iyer. Effector CD4+ T cells in health and disease 2007. Transworld Research Network, 2007.

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Alexander, Michael A. Immune-based cancer treatment: The T lymphocyte response. CRC Press, 2011.

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O'Leary, Paula Frances Gerardine. T cell influences in antibody responses to lipopolysaccharides and polysaccharides. University of Birmingham, 2000.

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Book chapters on the topic "T cells responses"

1

Munitic, Ivana, César Evaristo, Hsueh Cheng Sung, and Benedita Rocha. "Transcriptional Regulation during CD8 T-Cell Immune Responses." In Memory T Cells. Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-6451-9_2.

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Camus, Matthieu, and Jérôme Galon. "Memory T-Cell Responses and Survival in Human Cancer: Remember to Stay Alive." In Memory T Cells. Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-6451-9_13.

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Sieper, Joachim, and Jürgen Braun. "T cell responses in reactive and Lyme arthritis." In T Cells in Arthritis. Birkhäuser Basel, 1998. http://dx.doi.org/10.1007/978-3-0348-8823-3_9.

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Sieper, Joachim, and Jürgen Braun. "T cell responses in reactive and Lyme arthritis." In T Cells in Arthritis. Springer US, 1998. http://dx.doi.org/10.1007/978-1-4615-4285-8_9.

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Alderson, Kory L., and William J. Murphy. "Antigen Specific Memory T Cells and Their Putative Need for the Generation of Sustained Anti-Tumor Responses." In Memory T Cells. Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-6451-9_12.

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Young, Betty M., Susan Wiechert, Ruth A. Coleman, Prajwal Gurung, and Robert T. Cook. "Polyclonal and Antigen-specific Responses of T Cells and T Cell Subsets." In Alcohol. Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-242-7_19.

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Zingoni, Alessandra, Cristina Cerboni, Michele Ardolino, and Angela Santoni. "Modulation of T Cell-Mediated Immune Responses by Natural Killer Cells." In Natural Killer Cells. Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-642-02309-5_17.

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Maltzman, Jonathan S., Angus Thomson, and David M. Rothstein. "T cells and the principles of immune responses." In Transplant Immunology. John Wiley & Sons, Ltd, 2015. http://dx.doi.org/10.1002/9781119072997.ch6.

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Tournilhac, Olivier, and Peter Dreger. "Chronic Lymphocytic Leukaemia." In The EBMT/EHA CAR-T Cell Handbook. Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-94353-0_14.

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AbstractAlthough chronic lymphocytic leukaemia (CLL) was one of the first two entities in which CAR-T cells were evaluated, it has not yet arrived in the clinical routine. Since the landmark study by Porter et al. (2011), only six CLL-specific clinical trials have been published, altogether comprising no more than 155 patients (Porter et al. 2015; Gill et al. 2018; Turtle et al. 2017; Gauthier et al. 2020; Siddiqi et al. 2020; Wierda et al. 2020; Frey et al. 2020). All six of these studies investigated CD19-directed CAR-T constructs in heavily pretreated patients, mostly having failed BTKi+/− venetoclax therapy. Despite overall response rates of 60–95%, including MRD clearance in a large proportion of patients, the CR rates appear to be relatively low, and only a few durable responses have been reported in patients achieving a CR (Porter et al. 2015; Frey et al. 2020; Cappell et al. 2020). While toxicity includes 5–20% grade 3 cytokine release syndrome and 5–25% grade 3 neurotoxicity and appears manageable, long-term efficacy remains an unresolved issue. CLL-specific efficacy barriers for CD19 CAR-T cells could include a reduced capacity for sustained T cell expansion in extensively pretreated elderly CLL patients (Lemal and Tournilhac 2019), along with impaired T cell motility, impaired T cell mitochondrial fitness, and T cell exhaustion (Bair and Porter 2019). Concurrent use of ibrutinib might reduce the CRS rate and severity (Gauthier et al. 2020; Gill et al. 2018; Wierda et al. 2020) without impairing CAR-T cell expansion.
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Mage, Rose G., and Claire Rogel-Gaillard. "Immunogenetics in the rabbit." In The genetics and genomics of the rabbit. CABI, 2021. http://dx.doi.org/10.1079/9781780643342.0005.

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Abstract This chapter on immunogenetics in the rabbit focused on some genes with genetic and genomic sequence information including those encoding: soluble circulating immunoglobulin molecules (Igs) and their surface-bound forms on B lymphocytes (BCRs); T-cell receptors on T lymphocyte surfaces, (TCRs); the rabbit Leukocyte Antigen (RLA) complex (proteins on cells that function to present antigen fragments to TCRs); and some cytokine genes that encode key regulators of T- and B-cell responses.
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Conference papers on the topic "T cells responses"

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Pillay, Janesh, Vera M. Kamp, Tjaakje Visser, et al. "Myeloid Derived Suppressor Cells Inhibit T-cell Responses In Critically Ill Patients." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a6148.

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Rastogi, Ichwaku, and Douglas McNeel. "271 B cell primed CD8 T cells generate similar phenotype, function and anti-tumor responses to DC primed CD8 T cells." In SITC 37th Annual Meeting (SITC 2022) Abstracts. BMJ Publishing Group Ltd, 2022. http://dx.doi.org/10.1136/jitc-2022-sitc2022.0271.

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Wallington, Joshua, Anthony P. Williams, Karl J. Staples, and Tom M. A. Wilkinson. "Cytotoxic responses of mucosal-associated Invariant T cells to NTHi infection." In ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.pa2621.

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Kedmi, Ranit, Kai Mesa, and Dan Littman. "Abstract B167: Antigen-presenting cells as coordinators of T-cell responses to gut microbiota." In Abstracts: Fourth CRI-CIMT-EATI-AACR International Cancer Immunotherapy Conference: Translating Science into Survival; September 30 - October 3, 2018; New York, NY. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/2326-6074.cricimteatiaacr18-b167.

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Kamran, Neha, Hikmat Assi, Marianela Candolfi, et al. "Abstract 1085: Glioma-infiltrating myeloid derived suppressor cells inhibit anti-tumor T cell responses." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-1085.

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Lin, Ko Wei, Takeshi Nakajima, Kai Yu Jen, Erika C. Crouch, David L. Perkins, and Patricia W. Finn. "Surfactant Protein D Modulation Of Adaptive Immune Responses: Role Of T Cells." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a5161.

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Gavin, Marc A., Alexander Gragerov, Erik Espling, et al. "Abstract B45: Phosphatidylserine suppresses T cells through GPR174, and co-inhibition of adenosine receptors and GPR174 synergistically enhances T cell responses." In Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; November 17-20, 2019; Boston, MA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/2326-6074.tumimm19-b45.

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Kamran, Neha, Youping Li, Mariela Moreno-Ayala, et al. "Abstract 457: Depletion of glioma infiltrating myeloid derived suppressor cells promotes anti-tumor T cell responses." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-457.

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Wang, Zhaoming, and George J. Weiner. "Abstract 1687: T cells are required to maintain anti-CD20-mediated NK cell responses in vitro." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-1687.

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Szylar, G., and J. Brown. "S10 Suppression of macrophage inflammatory responses to streptococcus pneumoniae by regulatory t cells." In British Thoracic Society Winter Meeting 2017, QEII Centre Broad Sanctuary Westminster London SW1P 3EE, 6 to 8 December 2017, Programme and Abstracts. BMJ Publishing Group Ltd and British Thoracic Society, 2017. http://dx.doi.org/10.1136/thoraxjnl-2017-210983.16.

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Reports on the topic "T cells responses"

1

Wong, Jr, and K. K. Regulatory T Cells and Host Anti-CML Responses. Defense Technical Information Center, 2008. http://dx.doi.org/10.21236/ada487614.

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Wong, Jr, and K. K. Regulatory T Cells and Host Anti-CML Responses. Defense Technical Information Center, 2009. http://dx.doi.org/10.21236/ada510759.

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Beg, Amer A. Potentiation of T Lymphocyte Responses by Modulating NF-kB Activity in Dendritic Cells. Defense Technical Information Center, 2004. http://dx.doi.org/10.21236/ada437633.

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Beg, Amer A. Potentiation of T Lymphocyte Responses by Modulating NF - Kappa Beta Activity in Dendritic Cells. Defense Technical Information Center, 2003. http://dx.doi.org/10.21236/ada417929.

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Baszler, Timothy, Igor Savitsky, Christopher Davies, Lauren Staska, and Varda Shkap. Identification of bovine Neospora caninum cytotoxic T-lymphocyte epitopes for development of peptide-based vaccine. United States Department of Agriculture, 2006. http://dx.doi.org/10.32747/2006.7695592.bard.

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The goal of the one-year feasibility study was to identify specific cytotoxic T-lymphocyte (CTL) epitopes to Neosporacaninum in the natural bovine host in order to make progress toward developing an effective peptide-based vaccine against bovine neosporosis. We tested the hypothesis that: N. caninum SRS2 peptides contain immunogenicCTLepitope clusters cross-presented by multiple bovine MHC-I and MHC-IIhaplotypes. The specific objectives were: (1) Map bovine CTLepitopes of N. caninum NcSRS-2 and identify consensus MHC-I and class-II binding motifs; and (2) Determine if subunit immunization with peptides containing N. caninum-specificCTLepitopes cross-reactive to multiple bovine MHChaplotypes induces a CTL response in cattle with disparate MHChaplotypes. Neosporosis is a major cause of infectious abortion and congenital disease in cattle, persisting in cattle herds via vertical transmission.5 N. caninum abortions are reported in Israel; a serological survey of 52 Israeli dairy herds with reported abortions indicated a 31% infection rate in cows and 16% infection rate in aborted fetuses.9,14 Broad economic loss due to bovine neosporosis is estimated at $35,000,000 per year in California, USA, and $100,000,000 (Australian) per year in Australia and New Zealand.13 Per herd losses in a Canadian herd of 50 cattle are estimated more conservatively at $2,305 (Canadian) annually.4 Up to date practical measures to reduce losses from neosporosis in cattle have not been achieved. There is no chemotherapy available and, although progress has been made toward understanding immunity to Neospora infections, no efficacious vaccine is available to limit outbreaks or prevent abortions. Vaccine development to prevent N. caninum abortion and congenital infection remains a high research priority. To this end, our research group has over the past decade: 1) Identified the importance of T-lymphocyte-mediated immunity, particularly IFN-γ responses, as necessary for immune protection to congenital neosporosis in mice,1,2,10,11 and 2) Identified MHC class II restricted CD4+ CTL in Neosporainfected Holstein cattle,16 and 3) Identified NcSRS2 as a highly conserved surface protein associated with immunity to Neospora infections in mice and cattle.7,8,15 In this BARD-funded 12 month feasibility study, we continued our study of Neospora immunity in cattle and successfully completed T-lymphocyte epitope mapping of NcSRS2 surface protein with peptides and bovine immune cells,15 fulfilling objective 1. We also documented the importance of immune responses NcSRS2 by showing that immunization with native NcSRS2 reduces congenital Neospora transmission in mice,7 and that antibodies to NcSRS2 specifically inhibition invasion of placental trophoblasts.8 Most importantly we showed that T-lymphocyte responses similar to parasite infection, namely induction of activated IFN-γ secreting Tlymphocytes, could be induced by subunit immunization with NcSRS2 peptides containing the Neospora-specificCTLepitopes (Baszler et al, In preparation) fulfilling objective 2. Both DNA and peptide-based subunit approaches were tested. Only lipopeptide-based NcSRS2 subunits, modified with N-terminal linked palmitic acid to enhance Toll-like receptors 2 and 1 (TLR2-TLR1), stimulated robust antigen-specific T-lymphocyte proliferation, IFN-γ secretion, and serum antibody production across different MHC-IIhaplotypes. The discovery of MHC-II cross-reactive T-cellinducing parasite peptides capable of inducing a potentially protective immune response following subunit immunization in cattle is of significant practical importance to vaccine development to bovine neosporosis. In addition, our findings are more widely applicable in future investigations of protective T-cell, subunit-based immunity against other infectious diseases in outbred cattle populations.
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Fluhr, Robert, and Maor Bar-Peled. Novel Lectin Controls Wound-responses in Arabidopsis. United States Department of Agriculture, 2012. http://dx.doi.org/10.32747/2012.7697123.bard.

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Innate immune responses in animals and plants involve receptors that recognize microbe-associated molecules. In plants, one set of this defense system is characterized by large families of TIR–nucleotide binding site–leucine-rich repeat (TIR-NBS-LRR) resistance genes. The direct interaction between plant proteins harboring the TIR domain with proteins that transmit and facilitate a signaling pathway has yet to be shown. The Arabidopsis genome encodes TIR-domain containing genes that lack NBS and LRR whose functions are unknown. Here we investigated the functional role of such protein, TLW1 (TIR LECTIN WOUNDRESPONSIVE1). The TLW1 gene encodes a protein with two domains: a TIR domain linked to a lectin-containing domain. Our specific aim in this proposal was to examine the ramifications of the TL1-glycan interaction by; A) The functional characterization of TL1 activity in the context of plant wound response and B) Examine the hypothesis that wounding induced specific polysaccharides and examine them as candidates for TL-1 interactive glycan compounds. The Weizmann group showed TLW1 transcripts are rapidly induced by wounding in a JA-independent pathway and T-DNA-tagged tlw1 mutants that lack TLW1 transcripts, fail to initiate the full systemic wound response. Transcriptome methodology analysis was set up and transcriptome analyses indicates a two-fold reduced level of JA-responsive but not JA-independent transcripts. The TIR domain of TLW1 was found to interact directly with the KAT2/PED1 gene product responsible for the final b-oxidation steps in peroxisomal-basedJA biosynthesis. To identify potential binding target(s) of TL1 in plant wound response, the CCRC group first expressed recombinant TL1 in bacterial cells and optimized conditions for the protein expression. TL1 was most highly expressed in ArcticExpress cell line. Different types of extraction buffers and extraction methods were used to prepare plant extracts for TL1 binding assay. Optimized condition for glycan labeling was determined, and 2-aminobenzamide was used to label plant extracts. Sensitivity of MALDI and LC-MS using standard glycans. THAP (2,4,6- Trihydroxyacetophenone) showed minimal background peaks at positive mode of MALDI, however, it was insensitive with a minimum detection level of 100 ng. Using LC-MS, sensitivity was highly increased enough to detect 30 pmol concentration. However, patterns of total glycans displayed no significant difference between different extraction conditions when samples were separated with Dionex ICS-2000 ion chromatography system. Transgenic plants over-expressing lectin domains were generated to obtain active lectin domain in plant cells. Insertion of the overexpression construct into the plant genome was confirmed by antibiotic selection and genomic DNA PCR. However, RT-PCR analysis was not able to detect increased level of the transcripts. Binding ability of azelaic acid to recombinant TL1. Azelaic acid was detected in GST-TL1 elution fraction, however, DHB matrix has the same mass in background signals, which needs to be further tested on other matrices. The major findings showed the importance of TLW1 in regulating wound response. The findings demonstrate completely novel and unexpected TIR domain interactions and reveal a control nexus and mechanism that contributes to the propagation of wound responses in Arabidopsis. The implications are to our understanding of the function of TIR domains and to the notion that early molecular events occur systemically within minutes of a plant sustaining a wound. A WEB site (http://genome.weizmann.ac.il/hormonometer/) was set up that enables scientists to interact with a collated plant hormone database.
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Medof, M. E. Augmentation of Antitumor T-Cell Responses by Increasing APC T-Cell C5a/C3a-C5aR/C3aR Interactions. Defense Technical Information Center, 2013. http://dx.doi.org/10.21236/ada585489.

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Palmer, Guy, Varda Shkap, Wendy Brown, and Thea Molad. Control of bovine anaplasmosis: cytokine enhancement of vaccine efficacy. United States Department of Agriculture, 2007. http://dx.doi.org/10.32747/2007.7695879.bard.

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Anaplasmosis an arthropod-born disease of cattle caused by the rickettsia Anaplasma marginale and is an impediment to efficient production of healthy livestock in both Israel and the United States. Currently the only effective vaccines are derived from the blood of infected cattle. The risk of widespread transmission of both known and newly emergent pathogens has prevented licensure of live blood-based vaccines in the U.S. and is a major concern for their continued use in Israel. Consequently development of a safe, effective vaccine is a high priority. In this collaborative project we focused on two approaches to vaccine development. The first focused o n improving antigen delivery to livestock and specifically examined how DNA vaccines could be improved to enhance priming and expansion of the immune response. This research resulted in development and testing of two novel vaccine delivery systems--one that targeted antigen spread among dendritic cells (the key cell in priming immune responses and a follow-on construct that also specifically targeted antigen to the endosomal-lysosomal compartment the processing organelle within the dendritic cell that directs vaccine antigen to the MHC class ll-CD4* T cell priming pathway). The optimized construct targeting vaccine antigen to the dendritic cell MHC class II pathway was tested for ability to prime A. marginale specific immune responses in outbred cattle. The results demonstrated both statistically significant effects of priming with a single immunization, continued expansion of the primary immune response including development of high affinity lgG antibodies and rapid recall of the memory response following antigen challenge. This portion of the study represented a significant advance in vaccine delivery for livestock. Importantly the impact of these studies is not limited to A. marginale a s the targeting motifs are optimized for cattle and can be adapted to other cattle vaccinations by inserting a relevant pathogen-specific antigen. The second approach (which represented an addition to the project for which approval was requested as part of the first annual report) was a comparative approach between A . marginale and the Israel A . centrale vaccines train. This addition was requested as studies on Major Surface Protein( MSP)- 2 have shown that this antigen is highly antigenically variable and presented solely as a "static vaccine" antigen does not give cross-strain immunity. In contrast A. . centrale is an effective vaccine which Kimron Veterinary institute has used in the field in Israel for over 50 years. Taking advantage of this expertise, a broad comparison of wild type A. marginale and vaccine strain was initiated. These studies revealed three primary findings: i) use of the vaccine is associated with superinfection, but absence of clinical disease upon superinfection with A. marginale; ii) the A. centrale vaccine strain is not only less virulent but transmission in competent in Dermacentor spp. ticks; and iii) some but not all MSPs are conserved in basic orthologous structure but there are significant polymorphisms among the strains. These studies clearly indicated that there are statistically significant differences in biology (virulence and transmission) and provide a clear path for mapping of biology with the genomes. Based on these findings, we initiated complete genome sequencing of the Israel vaccine strain (although not currently funded by BARD) and plant to proceed with a comparative genomics approach using already sequenced wild-type A. marginale. These findings and ongoing collaborative research tie together filed vaccine experience with new genomic data, providing a new approach to vaccine development against a complex pathogen.
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Eldar, Avigdor, and Donald L. Evans. Streptococcus iniae Infections in Trout and Tilapia: Host-Pathogen Interactions, the Immune Response Toward the Pathogen and Vaccine Formulation. United States Department of Agriculture, 2000. http://dx.doi.org/10.32747/2000.7575286.bard.

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In Israel and in the U.S., Streptococcus iniae is responsible for considerable losses in various fish species. Poor understanding of its virulence factors and limited know-how-to of vaccine formulation and administration are the main reasons for the limited efficacy of vaccines. Our strategy was that in order to Improve control measures, both aspects should be equally addressed. Our proposal included the following objectives: (i) construction of host-pathogen interaction models; (ii) characterization of virulence factors and immunodominant antigens, with assessment of their relative importance in terms of protection and (iii) genetic identification of virulence factors and genes, with evaluation of the protective effect of recombinant proteins. We have shown that two different serotypes are involved. Their capsular polysaccharides (CPS) were characterized, and proved to play an important role in immune evasion and in other consequences of the infection. This is an innovative finding in fish bacteriology and resembles what, in other fields, has become apparent in the recent years: S. iniae alters surface antigens. By so doing, the pathogen escapes immune destruction. Immunological assays (agar-gel immunodiffusion and antibody titers) confirmed that only limited cross recognition between the two types occurs and that capsular polysaccharides are immunodominant. Vaccination with purified CPS (as an acellular vaccine) results in protection. In vitro and ex-vivo models have allowed us to unravel additional insights of the host-pathogen interactions. S. iniae 173 (type II) produced DNA fragmentation of TMB-8 cells characteristic of cellular necrosis; the same isolate also prevented the development of apoptosis in NCC. This was determined by finding reduced expression of phosphotidylserine (PS) on the outer membrane leaflet of NCC. NCC treated with this isolate had very high levels of cellular necrosis compared to all other isolates. This cellular pathology was confirmed by observing reduced DNA laddering in these same treated cells. Transmission EM also showed characteristic necrotic cellular changes in treated cells. To determine if the (in vitro) PCD/apoptosis protective effects of #173 correlated with any in vivo activity, tilapia were injected IV with #173 and #164 (an Israeli type I strain). Following injection, purified NCC were tested (in vitro) for cytotoxicity against HL-60 target cells. Four significant observations were made : (i) fish injected with #173 had 100-400% increased cytotoxicity compared to #164 (ii) in vivo activation occurred within 5 minutes of injection; (iii) activation occurred only within the peripheral blood compartment; and (iv) the isolate that protected NCC from apoptosis in vitro caused in vivo activation of cytotoxicity. The levels of in vivo cytotoxicity responses are associated with certain pathogens (pathogen associated molecular patterns/PAMP) and with the tissue of origin of NCC. NCC from different tissue (i.e. PBL, anterior kidney, spleen) exist in different states of differentiation. Random amplified polymorphic DNA (RAPD) analysis revealed the "adaptation" of the bacterium to the vaccinated environment, suggesting a "Darwinian-like" evolution of any bacterium. Due to the selective pressure which has occurred in the vaccinated environment, type II strains, able to evade the protective response elicited by the vaccine, have evolved from type I strains. The increased virulence through the appropriation of a novel antigenic composition conforms with pathogenic mechanisms described for other streptococci. Vaccine efficacy was improved: water-in-oil formulations were found effective in inducing protection that lasted for a period of (at least) 6 months. Protection was evaluated by functional tests - the protective effect, and immunological parameters - elicitation of T- and B-cells proliferation. Vaccinated fish were found to be resistant to the disease for (at least) six months; protection was accompanied by activation of the cellular and the humoral branches.
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Banai, Menachem, and Gary Splitter. Molecular Characterization and Function of Brucella Immunodominant Proteins. United States Department of Agriculture, 1993. http://dx.doi.org/10.32747/1993.7568100.bard.

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The BARD project was a continuation of a previous BARD funded research project. It was aimed at characterization of the 12kDa immunodominant protein and subsequently the cloning and expression of the gene in E. coli. Additional immunodominant proteins were sought among genomic B. abortus expression library clones using T-lymphocyte proliferation assay as a screening method. The 12kDa protein was identified as the L7/L12 ribosomal protein demonstrating in the first time the role a structural protein may play in the development of the host's immunity against the organism. The gene was cloned from B. abortus (USA) and B. melitensis (Israel) showing identity of the oligonucleotide sequence between the two species. Further subcloning allowed expression of the protein in E. coli. While the native protein was shown to have DTH antigenicity its recombinant analog lacked this activity. In contrast the two proteins elicited lymphocyte proliferation in experimental murine brucellosis. CD4+ cells of the Th1 subset predominantly responded to this protein demonstrating the development of protective immunity (g-IFN, and IL-2) in the host. Similar results were obtained with bovine Brucella primed lymphocytes. UvrA, GroE1 and GroEs were additional Brucella immunodominant proteins that demonstrated MHC class II antigenicity. The role cytotoxic cells are playing in the clearance of brucella cells was shown using knock out mice defective either in their CD4+ or CD8+ cells. CD4+ defective mice were able to clear brucella as fast as did normal mice. In contrast mice which were defective in their CD8+ cells could not clear the organisms effectively proving the importance of this subtype cell line in development of protective immunity. The understanding of the host's immune response and the expansion of the panel of Brucella immunodominant proteins opened new avenues in vaccine design. It is now feasible to selectively use immunodominant proteins either as subunit vaccine to fortify immunity of older animals or as diagnostic reagents for the serological survaillance.
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